Fig. 10From: Trophoblast-derived miR-410-5p induces M2 macrophage polarization and mediates immunotolerance at the fetal-maternal interface by targeting the STAT1 signaling pathwaySchematic illustration of trophoblast-derived miR-410-5p inhibition of STAT1 regulating macrophage polarization at the fetal-maternal interface. Trophoblast-derived EXOs-miR-410-5p purposefully inhibits the intracellular activation of STAT1, reduces the accumulation of ROS, and prevents mitochondrial depolarization. Simultaneously, miR-410-5p further promoted FAO in cells, increased the secretion of MDC and TARC, ultimately induced M2 polarization, and participated in the maintenance of maternal–fetal interface immune homeostasisBack to article page